We propose to investigate a previously undescribed mechanism which produces large increases in blood flow in the hind limb of rabbits. These increases result from large reductions in vascular resistance, but they are not due to a release of Alpha-adrenergic vasoconstrictor tone. We conclude from preliminary evidence that the blood flow increases are due to an active muscle vasodilatation which we activated by stimulating in the perifornicular region of the hypothalamus. Although sympathetic active muscle vasodilatation is described in carnivores, the existence of such a phenomenon in rabbits has been categorically denied in the past. Therefore, we have proposed experiments to confirm that the vasodilatation occurs specifically within the skeletal muscle vasculature and that it is mediated by the sympathetic nervous system. Unlike carnivores, the peripheral mediator of this vasodilatation in rabbits is not acetyl-choline. Thus, we have proposed protocols to screen a variety of putative neurotransmitters in an attempt to identify the postganglionic mediator of this vasodilatation. The integrity of this vasodilatory pathway in the central nervous system may be dependent upon Beta-adrenergic mechanisms because in our preliminary experiments, the intrahypothalamic administration of minute amounts of propranolol could abolish the vasodilatation. We have also proposed a series of experiments designed to clarify the nature of these central mechanisms which, in the long term, may aid in the understanding of the clinical applications of propranolol.